An animal model system has been developed which permits studies of the absorption, excretion and body distribution of lead at intervals after the administration of either oral or parenteral doses of radiolead. An inverse relationship between lead retention and dietary calcium content has been known to exist for many years but the reasons for this association remained unknown. In rats, the manipulation of dietary calcium had no significant effect upon the absorption of lead but calcium-deprived animals had decreased excretion and thus increased body retention of lead. Intraluminal calcium decreased the absorption of test doses of lead from the small intestine in a dose-related manner. We postulated that this occurred because the two metals competed for similar binding sites on intestinal mucosal proteins which were important in the absorptive process. In vivo, lead bound to heat-stable intestinal mucosal fractions which have been shown to bind calcium. Although more lead bound to the higher molecular weight fraction and more calcium bound to the lower molecular weight vitamin D-induced calcium binding protein, substantial amounts of lead and calcium were found in both fractions. Further, the addition of calcium to test dose of lead markedly diminished the amount of lead bound by both fractions. Shared binding sites on absorptive proteins would explain why dietary calcium decreases lead absorption. These proteins seem also to bind other metals such as iron and cobalt. Studies are in progress to determine if they explain the inter-relationships which exist between the absorption of divalent metals.